The proposed research concerns the mechanisms of Na-Ca interactions in intestinal and vascular smooth muscle. The smooth muscle preparations are the isolated guinea taenia coli, the rabbit aorta and the dog coronary artery. I will test the hypothesis of the plasmalemmal Na-Ca exchange carrier in a definitive way by measuring: 1. 45 Ca efflux and net Ca extrusion as a function of external Na concentration (Na ion), 2. Ca influx and net uptake as a function of Na ion in, 3. 22Na efflux and net extrusion as a function of (Ca ions) and 4. Na influx and net uptake as a function of (Ca ions) in. These experiments have become practical in my laboratory because of our long experience with measuring cellular Ca and my recent significant improvements of the quenching techniques for measuring both total intracellular Na ion and Ca ions. Using these techniques we are able to accurately measure the rate constant for net Ca extrusion against the electrochemical gradient from Ca loaded smooth muscle cells. This "active" Ca extrusion will be quantitated with resepct to: 1. the electrochemical Na ion gradient, b. cellular ATP, c. cellular cyclic AMP, d. temperature, 3. electrochemical Ca ions gradient. In addition I will test the effect of intracellular Na on agonist sensitive cellular Ca compartments. The proposed research will provide a much needed quantitative description of the active Ca transport mechanism and its modulation by Na ions and a better understanding of Na-Ca interactions at other sites and their role in the control of smooth muscle contractility. This information will be of great importance in our understanding of the etilogy of clinical hypertension.